Lansoprazole Tablets

Mechanism

Lansoprazole irreversibly binds to and inhibits the gastric proton pump (H+/K+ ATPase), blocking the final step of acid secretion. This results in profound and sustained reduction of gastric acid production.

Pharmacokinetics

• Absorption: Rapid oral absorption; bioavailability ≈ 80–90%
• Distribution: Widely distributed; plasma protein binding ≈ 97%
• Metabolism: Extensively metabolized in the liver via CYP2C19 and CYP3A4
• Elimination: Renal and fecal excretion of metabolites
• Half-life: ≈ 1.5–2 hours (effect lasts longer due to irreversible binding)

Side Effects

• Headache
• Nausea
• Diarrhea
• Abdominal pain
• Long-term use: risk of hypomagnesemia, vitamin B12 deficiency, osteoporosis-related fractures

Contraindication

• Hypersensitivity to Lansoprazole or other PPIs
• Concomitant use with rilpivirine-containing products
• Severe hepatic impairment (use cautiously)

Interaction

• Clopidogrel — reduced activation due to CYP2C19 inhibition
• Ketoconazole, itraconazole — reduced absorption due to decreased gastric acidity
• Warfarin — may increase INR, monitor closely
• Digoxin — increased absorption, monitor levels
• Other PPIs — additive acid suppression

Warning and Precautions

• Long-term use may lead to hypomagnesemia, vitamin B12 deficiency, and osteoporosis-related fractures.
• Use cautiously in patients with severe hepatic impairment.
• Monitor for gastrointestinal infections (e.g., *Clostridium difficile*) due to reduced gastric acidity.
• Prolonged therapy may increase risk of chronic kidney disease and fundic gland polyps.
• Discontinue if hypersensitivity reactions occur.
• Use with caution in patients taking drugs dependent on gastric pH for absorption (e.g., antifungals, antivirals).